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As central regulation is important for bone metabolism, HPD\u2010sheep develop severe osteoporosis because of low bone turnover. In this study we investigated metaphyseal fracture healing in HPD\u2010sheep. To elucidate potential pathomechanisms, we included a treatment group receiving thyroxine T4 and 17\u03b2\u2010estradiol. Because clinically osteoporotic fractures often occur in the bone metaphysis, HPD\u2010sheep and healthy controls received an osteotomy in the distal femoral condyle. Half of the HPD\u2010sheep were systemically treated with thyroxine T4 and 17\u03b2\u2010estradiol during the healing period. Fracture healing was evaluated after 8 weeks using pQCT, \u00b5CT, and histomorphometrical analysis. Bone mineral density (BMD) and bone volume\/total volume (BV\/TV) were considerably reduced by 30% and 36%, respectively, in the osteotomy gap of the HPD\u2010sheep compared to healthy sheep. Histomorphometry also revealed a decreased amount of newly formed bone (\u221229%) and some remaining cartilage in the HPD\u2010group, suggesting that HPD disturbed fracture healing. Thyroxine T4 and 17\u03b2\u2010estradiol substitution considerably improved bone healing in the HPD\u2010sheep. Our results indicate that fracture healing requires central regulation and that thyroxine T4 and 17\u03b2\u2010estradiol contribute to the complex pathomechanisms of delayed metaphyseal bone healing in HPD\u2010sheep. \u00a9 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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